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Questions Q55.1 How do salicylic acid and α-hydroxy acids differ regarding lipid solubility and the resultant depth of percutaneous absorption? (Pg. 608) Q55.2 What are some of the mechanisms of salicylic acid leading to keratolytic and desmolytic effects? (Pg. 608) Q55.3 What types of patients may be considered for field therapy for actinic keratosis with 0.5% 5-fluorouracil/10% salicylic acid cream? (Pg. 610) Q55.4 What are several…

Questions Q54.1 What are the four main stages (and their general sequence) of wound healing? (Pg. 598) Q54.2 What are some of the most important medical conditions to exclude (and related laboratory tests) in patients with a chronic cutaneous ulcer? (Pgs. 598, 600 Table 54.1 ) Q54.3 What are some of the main clinical features to distinguish the most common causes of cutaneous ulcers? (Pgs. 598,…

Questions Q53.1 What depth of peel is generated using superficial, intermediate, and deep chemical peels? What does frosting during a chemical peel indicate? (Pgs. 592, 593×2, Tables 53.1 and 53.2 ) Q53.2 Why does salicylic acid (SA) penetrate comedones better than other superficial chemical peels? What are additional benefits of SA peels? (Pg. 593) Q53.3 What are the components of Jessner’s peel? (Pg. 593×2, Table 53.3…

Questions Q52.1 What are the primary epidermal and dermal effects from α-hydroxy acids (AHA) that lead to clinical benefit in various cutaneous disorders? ( Pg. 586×2 ) Q52.2 What are examples of the polyhydroxy acids (PHA), and what advantage do these chemicals offer compared with the α-hydroxy acids? ( Pgs. 587, 588 ) Q52.3 What are the primary microscopic and clinical differences noted with photodamaged skin…

Questions Q51.1 What are the major scalp conditions commonly treated with therapeutic shampoos? (Pg. 576) Q51.2 What is the evidence for the role of Pityrosporum yeast in the pathogenesis of seborrheic dermatitis, and which shampoo ingredients reduce its growth? (Pg. 578) Q51.3 What are the primary mechanisms of action by which therapeutic shampoos treat scalp conditions? (Pg. 578) Q51.4 Which factors play the most important role…

Questions Q50.1 What are the key concepts covered by the most recent US Food and Drug Administration (FDA) monographs on sunscreens? (Pg. 566) Q50.2 Concerning ultraviolet B (UVB) filters, (1) which are the two most potent current UVB absorbers (filters), and (2) why has para-aminobenzoic acid (PABA) use declined? (Pg. 567×2) Q50.3 What ultraviolet A (UVA) filters have the broadest coverage (including significant absorption of UVA-1)…

Questions Q49.1 Which cells in the skin have vitamin D receptors? In the most general sense, what is the biologic impact of vitamin D on these cells? (Pg. 557) Q49.2 What are the major steps (and sites in the body) for conversion of provitamin D 3 through 1,2-hydroxy vitamin D 3 ? (Pg. 558, Fig. 49.1 ) Q49.3 At the molecular level how does vitamin D…

Questions Q48.1 Concerning the mechanism of action for topical tacrolimus and pimecrolimus, what aspects are the most applicable to patients with atopic dermatitis? (Pgs. 550, 554) Q48.2 What is/are the official indication(s) for topical calcineurin inhibitors from (1) the US Food and Drug Administration (FDA), and (2) the Canadian, and (3) European Union governing bodies? (Pg. 550×3) Q48.3 From the meta-analyses and reviews cited in the…

Questions Q47.1 What is the evidence for the success of topical 5-fluorouracil (5-FU) in the treatment of actinic keratoses? (Pg. 543) Q47.2 How should topical 5-FU be used to treat nonmelanoma skin cancer? (Pg. 543) Q47.3 Which inherited enzyme deficiency significantly increases the risk of toxicity with 5-FU therapy? (Pgs. 543, 544) Q47.4 What commercial product(s) are suitable alternatives for compounded nitrogen mustard? (Pg. 544) Q47.5…

Questions Q46.1 Concerning topical retinoids in this chapter, what are (1) the three naturally occurring retinoids, (2) the three synthetic retinoids, and (3) the metabolic differences likely because of this distinction? (Pg. 529, Table 46.1 ) Q46.2 Which of the topical retinoids have a traditional pregnancy rating (1) category D, and (2) category X? (Pg. 529, Table 46.3 ) Q46.3 Concerning the correlation of increased retinoid…

Questions Q45.1 What is the procedure for performing the Stoughton vasoconstriction assay, and how does this assay assess the potency of topical corticosteroid (TCS) molecules? (Pg. 512) Q45.2 How does the vehicle affect the potency of TCS? What are the pros and cons of including propylene glycol in the vehicle? (Pgs. 514, 522) Q45.3 At the molecular level, how does TCS induce production of various proteins…

Questions Q44.1 What is the mechanism of action for (1) permethrin, (2) ivermectin, (3) malathion, and (4) spinosad? (Pgs. 506, 507, 508) Q44.2 What is the first-line treatment for patients with scabies? (Pg. 506) Q44.3 What is the permethrin treatment protocol for patients infested with scabies? (Pg. 506) Q44.4 What specific plant contact sensitization predisposes patients to a cross-reaction with topical pyrethroids? (Pg. 506) Q44.5 What…

Questions Q43.1 What are the main steps for the mechanism of action for (1) acyclovir, and (2) penciclovir? (Pgs. 494, 496) Q43.2 What is the relative sensitivity of (1) acyclovir, and (2) penciclovir for various viruses in the human herpesvirus family? (Pgs. 494, 496) Q43.3 What are the clinical and mechanistic advantages of penciclovir compared with acyclovir? (Pg. 496×2) Q43.4 Describe a commonly used treatment protocol…

Questions Q42.1 What are primary examples of topical antifungal agents from the following categories: (1) polyenes, (2) azoles, (3) allylamines, (4) benzylamines, and (5) hydroxypyridones? (Pg. 480, Table 42.1 ) Q42.2 Although azole and allylamine antifungals both block ergosterol synthesis, how do they differ in their mechanism of action? (Pgs. 481, 486, Table 42.2 ) Q42.3 How does tavaborole differ from other antifungals in its mechanism…

Questions Q41.1 How effective is bacitracin versus mupirocin in eliminating nasal staphylococcal carriage? (Pgs. 466, 470) Q41.2 Concerning postoperative topical antibacterial use, (1) what are the pros and cons of routinely applying petrolatum versus a topical antibacterial agent for ‘clean’ dermatologic surgical wounds, and (2) how common is contact sensitization with bacitracin, neomycin, and mupirocin? (Pgs. 466, 468, 469, 470×2, 471) Q41.3 How common is anaphylaxis…

Questions Q40.1 What are several important drug interactions with anticholinergic drugs discussed in this chapter? ( Pg. 446) Q40.2 What are several factors which increase the risk of myopathy from attenuated androgens? (Pg. 447) Q40.3 What are some of the properties of biotin which led to its clinical use for hair and nail disorders? (Pg. 447) Q40.4 What is the most common adverse effect of clofazimine?…

Questions Q39.1 What is the most important adverse effect from the most potent bisphosphonates (such as etidronate)? (Pg. 431) Q39.2 What are the mechanisms of action by which bisphosphonates prevent and treat osteoporosis? (Pg. 431) Q39.3 What are the reasons that oral bisphosphonates must be taken in a fasting state and in an upright position? (Pg. 435) Q39.4 What are typical doses for (1) calcium, (2)…

Questions Q38.1 What are the US Food and Drug Administration (FDA)-approved indications for vismodegib and sonidegib? (Pg. 422×2) Q38.2 What are the various off-label uses for Hedgehog (Hh) pathway inhibitors? (Pgs. 423×4, 424×3) Q38.3 What are potential adverse effects of vismodegib and sonidegib? (Pgs. 424×3, 426, 427) Q38.4 What does the evidence suggest regarding Hh inhibitor risk to the embryo/fetus in pregnant females? (Pg. 424×2) Q38.5…

Questions Q37.1 What are several drugs commonly associated with mucositis? (Pgs. 406, 409, 414, 415×2, 416×2) Q37.2 Which drug class is most commonly associated with an acneiform papulopustular eruption? (Pg. 406) Q37.3 What is the time course of the papulopustular rash following the initiation of therapy with epidermal growth factor receptor inhibitor (EGFRI)? (Pg. 406) Q37.4 Before starting therapy with an EGFRI, what is the recommended…

Questions Q36.1 What are the mechanisms by which intravenous immunoglobulin (IVIg) affects (1) antibody (Ab) production, (2) Ab neutralization, (3) the complement system, (4) T-cell activation, (5) immune cell trafficking, and (6) Fas/Fas ligand interaction? (Pg. 398) Q36.2 What is the likelihood of success and unique risks when using IVIg for patients with severe, recalcitrant dermatomyositis? (Pg. 399) Q36.3 What is the likelihood of success and…